Bacterial invasion of the lower urinary tract commonly leads to incapacitating symptoms and ascending pyelonephritis. Despite antibiotics and corrective surgery, morbidity and mortality from urinary tract infections (UTI) are rising. In the oral cavity and gastrointestinal tract, bacterial adherence and subsequent tissue infection are directly related to the local immune response with locally-produced secretory IgA being the most important factor inhibiting bacterial adherence. Following UTI, urinary secretory IgA also increases. Experimental animals immunized by placing bacterial antigens into the bladder subsequently demonstrate decreased bacterial adherence. We hope to develop new methods of treating and preventing recurrent UTI by defining and increasing anti-adherence factors within the urinary tract. We have developed an assay using isotope-labelled bacteria which can quantitate bacterial adherence to mucosal surface of the bladder. With this assay, we will determine the factors and mechanisms which mediate urinary tract attachment, study IgA-bacterial interactions, extend bacterial adherence quantitation to urethra and vagina, and evaluate whether animals with decreased bacterial adherence are less susceptible to UTI.